尼莫地平对大鼠急性脑缺血再灌注损伤的作用机制研究  

The mechanism of nimodipine on acute cerebral ischemia-reperfusion injury in rats

作　　者：韩威[1,2,3] 张颖[4] 魏胜男[5] 孟昭杰 戴丽君[3] 

机构地区：[1]江苏大学进站 [2]江苏大学,江苏镇江212013 [3]吉林省脑科医院神经内科,吉林四平136000 [4]吉林大学白求恩第一医院神经内科,吉林长春130021 [5]吉林大学白求恩医学院药理学系,吉林长春130021

出　　处：《中风与神经疾病杂志》2013年第8期713-715,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨尼莫地平对急性脑缺血再灌注损伤的的早期保护作用。方法线栓法复制大鼠急性脑缺血模型。30只雄性Wistar大鼠随即分为假手术组、模型组、尼莫地平组3组。模型组采血2h再灌注2h。尼莫地平组大鼠在缺血0时刻起每小时腹腔注射给药一次,剂量为5mg/kg。各组大鼠在手术4h后实验结束后,行腹主动脉采血,同时取完整脑组织。Western blot检测各组大鼠脑组织中AMPK、磷酸化AMPK(p-AMPK)、Bax、活化的caspase-3蛋白(cleaved caspase-3)的表达。结果与模型组相比,尼莫地平组大鼠脑组织p-AMPK蛋白和casepase-3的表达明显下降,Bax表达显著高于模型组。结论尼莫地平对大鼠急性脑缺血再灌注损伤有保护作用,抑制体内缺血诱导的神经细胞凋亡,其作用与下调AMPK有关。Objective To investigate the early protective effect of nimodipine on acute cerebral ischemia reperfusion injury.Methods Focal cerebral inschemia/reperfusion was induced by the middle cerebral artery occlusion（MCAO） method.30 male Wistar rats were randomly divided into three groups（Sham Model Nimodipine treatment group）.The model group was induced by 2h ischemia following 2h reperfusion.The nimodipine treatment（5mg/kg） was given at the time of ischemia by intraperitoneal injection once an hour.At the end of the experiment,the abdominal aorta blood was obtained,and full brain tissue was saved.The expression of AMPK,p-AMPK.Bax、cleaved caspase-3 by Western blot of brain tissue was compared between groups.Results The expression of p-AMPK and casepase-3 of nimodipine treatment group was significantly decreased while Bax increased significantly compared with model group.Conclusion Nimodipine has a protective effect on acute cerebral ischemia reperfusion injury and inhibits nerve cell apoptosis,which is closely related to it＇s the reduction of AMPK.

关 键 词：尼莫地平 缺血再灌注损伤 AMPK BAX CASEPASE-3 

分 类 号：R743[医药卫生—神经病学与精神病学]